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The NuRD-SWI/SNF antagonism regulates the coordinated activation of EMT and inflammation in oral cancer

ABSTRACT: The NuRD-SWI/SNF antagonism regulates the coordinated activation of EMT and inflammation in oral cancer

PROVIDER: PRJNA1083586 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28217891_1.fastq.gz	Fastqsanger.gz
	SRR28217891_2.fastq.gz	Fastqsanger.gz
	SRR28217892_1.fastq.gz	Fastqsanger.gz
	SRR28217892_2.fastq.gz	Fastqsanger.gz
	SRR28217893_1.fastq.gz	Fastqsanger.gz

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The NuRD-SWI/SNF antagonism regulates the coordinated activation of EMT and inflammation in oral cancer

Project description:The NuRD-SWI/SNF antagonism regulates the coordinated activation of EMT and inflammation in oral cancer

| PRJNA1083503 | ENA

The NuRD-SWI/SNF antagonism regulates the coordinated activation of EMT and inflammation in oral cancer

Project description:Phenotypic plasticity and inflammation, two well-established hallmarks of cancer, play key roles in local invasion and distant metastasis by enabling rapid adaptation to dynamic micro-environmental changes. Here, we show that in oral squamous carcinoma cell carcinoma (OSCC), the competition between the NuRD and SWI/SNF chromatin remodeling complexes plays a pivotal role in regulating both epithelialmesenchymal plasticity (EMP) and inflammation. By genetically perturbing both complexes, we demonstrate their opposing downstream effects on inflammatory pathways and EMP regulation. In particular, downregulation of the BRG1-specific SWI/SNF complex deregulates key inflammatory genes such as TNF-α and IL6 in opposite ways when compared with loss of CDK2AP1, a key member of the NuRD complex. We show that CDK2AP1 genetic ablation triggers a pro-inflammatory secretome encompassing several chemo- and cytokines thus promoting the recruitment of monocytes into the tumor microenvironment (TME) and their differentiation into M2c macrophages, as also validated on tumor microarrays from OSCC patient-derived tumor samples. Further analysis of the inverse correlation between CDK2AP1 expression and TME immune infiltration revealed specific downstream effects on CD68+ macrophage abundance and localization. Our study sheds light on the role of chromatin remodeling complexes in OSCC locoregional invasion and points at the potential of CDK2AP1 and other members of the NuRD and SWI/SNF chromatin remodeling complexes as prognostic markers and therapeutic targets.

2025-06-27 | GSE260831 | GEO

The NuRD-SWI/SNF antagonism regulates the coordinated activation of EMT and inflammation in oral cancer

2025-06-27 | GSE260789 | GEO

DOC1-dependent recruitment of NURD reveals antagonism with SWI/SNF during epithelial-mesenchymal transition in oral cancer cells.

Project description:The Nucleosome Remodeling and Deacetylase (NURD) complex is a key regulator of cell differentiation that has also been implicated in tumorigenesis. Loss of the NURD subunit DOC1 is associated with human oral squamous cell carcinomas (OSCC). Here, we show that restoration of DOC1 expression in OSCC cells leads to a reversal of epithelial-mesenchymal transition (EMT). This is caused by the DOC1-dependent recruitment of NURD to repress the Twist master regulators of EMT. NURD recruitment drives extensive epigenetic reprogramming, including eviction of the SWI/SNF remodeler, formation of inaccessible chromatin, H3K27 deacetylation, recruitment of PRC2 and KDM1A, followed by H3K27 methylation and H3K4 demethylation. Strikingly, depletion of SWI/SNF mimics the effects of DOC1 re-expression. Our results suggest that SWI/SNF and NURD function antagonistically to control chromatin state. We propose that disturbance of this dynamic equilibrium may lead to defects in gene expression that drive human cancer.

2017-07-05 | GSE97839 | GEO

Functional antagonism of chromatin modulators regulates EMT

Project description:Functional antagonism of chromatin modulators regulates EMT

| PRJNA648646 | ENA

The impact of SWI/SNF and NuRD inactivation on gene expression is tightly coupled with levels of RNA Polymerase II occupancy at promoters

Project description:SWI/SNF and NuRD are protein complexes that antagonistically regulate DNA accessibility. However, repression of their activities often leads to unanticipated changes in target gene expression (paradoxical), highlighting our incomplete understanding of their activities. Here we show that SWI/SNF and NuRD are in a tug-of-war to regulate PRC2 occupancy at lowly expressed and bivalent genes in mESCs. In contrast, at promoters of average or highly expressed genes, SWI/SNF and NuRD antagonistically modulate RNA Polymerase II release kinetics, arguably via modifying H3.3 and H2A.Z turnover rates at promoter-flanking nucleosomes, leading to paradoxical changes in gene expression. Owing to this mechanism, the relative activities of the two remodelers potentiate gene promoters towards Pol II-dependent open or PRC2-dependent closed chromatin states. Our results highlight RNA Polymerase II occupancy as the primary parameter determining the direction of gene expression changes in response to SWI/SNF and NuRD inactivation at gene promoters in mESCs.

2023-01-19 | GSE206497 | GEO

Bulk RNA-seq of mouse colonic organoids: CRISPR functional Screening of Satb2-interact proteins (NuRD and SWI/SNF complex)

Project description:CRISPR knock out the NuRD and SWI/SNF complex gene from mouse colonic organoids to validate the potential function with SATB2.

2024-03-07 | GSE213878 | GEO

Functional antagonism of chromatin modulators regulates EMT [ChIP-Seq]

Project description:Functional antagonism of chromatin modulators regulates EMT [ChIP-Seq]

| PRJNA648647 | ENA

Functional antagonism of chromatin modulators regulates EMT [ATAC-Seq]

Project description:Functional antagonism of chromatin modulators regulates EMT [ATAC-Seq]

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SWI/SNF antagonism of the PRC2 mediates estrogen-induced progesterone receptor expression

Project description:SWI/SNF antagonism of the PRC2 mediates estrogen-induced progesterone receptor expression

| PRJNA800820 | ENA